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I'm going to talk to you about the hormone whose name you've heard many times – insulin. Even though this chapter is going to cover some technical points, I think you ought to read it carefully, because for many of you, the answers are here.

Almost everyone has heard of insulin because it's given to certain kinds of diabetics to help control their blood sugar levels. This insulin hormone is one of the most powerful and efficient substances that the body uses to control the use, distribution and storage of energy.

Your body is an energy machine, never resting, always metabolically active – and it powers its operations mainly through the use of glucose (a basic form of sugar) in the blood. It must have the glucose, and even under conditions of starvation it will continue to obtain it so long as there's anything in the body it can convert into glucose. Thus, even on a prolonged, total fast, the body can maintain its glucose level within a rather narrow normal range. As a general rule, of course, the body obtains its principal supply of fuel by eating.

Artwork by Paul Davies

Eating a Meal

Dinnertime comes. You sit down at the table and consume a three-course dinner. What does your body do? Somewhere between chewing and excreting, it absorbs certain substances from your food, mostly across the surface of your small intestine. At that moment, the food is actually entering your body for use.

From the carbohydrates you eat, your body will absorb simple sugars, all of which either are, or quickly and easily become, glucose.

From fats, it absorbs glycerol and fatty acids, and from proteins it absorbs amino acids, the building blocks of protein.

Obviously, if you eat a lot of carbohydrate, you'll produce a lot of glucose in your blood. Sounds good doesn't it? All that energy coursing through your system. Eat sugar and starches and fruits and you're going to get those blood sugar levels up fast, aren't you?

If you love candy bars, perhaps you're saying, "That's great, the more I eat, the stronger I'll be."

Alas, a bad mistake. You see, your body was designed way back in pre-Neanderthal days when they didn't have any candy bars. Your body's capacity to deal with unrefined foods as they occur in nature is quite adequate; its capacity to deal with an excess of quick-energy, simple sugars is pretty poor, which is the true reason why our 20th century diet gets us into trouble.

If you don't understand this yet, then let's look at what insulin and the other energy-controlling hormones do when you eat.

As Your Blood Glucose Rises

If your blood sugar levels go sharply up, as they do soon after you eat carbohydrate, your body makes an instant decision. How much of that pure energy is it going to use for immediate needs and how much will it store for future requirements?

The instrument of its decision is insulin, because insulin governs the processing of blood sugar.

Insulin is manufactured in a part of your pancreas called the islets of Langerhans. As the sugar in your blood goes up, insulin rushes forth and converts a portion of that glucose to glycogen, a starch stored in the muscles and the liver and readily available for energy use. If all the glycogen storage areas are filled, and there is still more glucose in the blood beyond that which the body needs to function, insulin will convert the excess to fatty tissue called triglyceride, which we carry on our bodies as the main chemical constituent of adipose tissue – the stuff you're reading this book to get rid of. That's why insulin has been called "the fat-producing hormone."

Insulin is a pretty efficient worker. If it were not, your body could not process glucose, its basic fuel, and blood glucose levels would escalate while the body searched for other fuels – first your fat stores, and then your muscle tissue itself. That's what happens in insulin-deficient diabetes when no insulin is present. On the other hand, suppose insulin is too effective, or in too great a supply. It would process too much, leaving too little to circulate in the blood to fuel the brain. The body attempts to adjust by liberating counterregulatory hormones – mainly glucagon, adrenocorticoids and adrenalin to raise the glucose level, but a stiff dose of insulin can overpower the lot of them. Fortunately for most of us, this glucose balancing act takes place automatically and our blood sugar stays in a fairly narrow, normal range of between 65 and 110 mg per 100 cc of blood.

Hyperinsulinism

It's easy to see that there's a relationship between the kinds of foods you eat and the amount of insulin in your bloodstream. Carbohydrate food, especially simple carbohydrates such as sugar, honey, milk and fruit, which contain glucose, and refined carbohydrates like flour, white rice, and potato starch, which, because they are readily absorbed through the gut, speedily convert to glucose, require a lot of insulin. Proteins and fats, on the other hand, produce almost no alteration in the insulin level.

As an overweight person becomes fatter the insulin problem expands too. Numerous studies have shown that the obese (and diabetic) individual is extremely unresponsive to the action of insulin. That's where you will see the term ''insulin resistance." Carbohydrates are triggering the release of large quantities of the hormone, but the body is incapable of utilising it efficiently. The body responds by putting out yet more insulin. Consequently overweight and high insulin levels are almost synonymous. And, to confuse the cart-before-the-horse issue a little more, it has been shown experimentally that high levels of insulin can themselves increase insulin resistance. This means that the high insulin levels can be the cause of the entire vicious carbohydrate – insulin – insulin resistance cycle.

What appears to happen is that the insulin receptors on the surfaces of the body's cells are blocked from carrying out their function, which in turn prevents insulin from stimulating the transfer of glucose to the cells for energy use. It's one reason why overweight individuals are tired much of the time. Because insulin is not effective in converting glucose into energy, it transfers more and more into stored fat. You'd like to slim down, but your body is in fact, becoming a fat-producing machine.

Your body's hormonal system is now in desperate straits. Insulin – your fat producing hormone – is now being secreted all the time to deal with high sugar levels, and it is doing its job less and less effectively. In time, even the insulin receptors that convert glucose to fat start getting worn out – this forecasts diabetes. In severe cases, the pancreas itself becomes exhausted by the effort required to produce so much insulin and a high-insulin diabetes changes into the insulin-dependent type.

To have your insulin levels more or less permanently high and yet to be resistant to the effects of insulin is what's called hyperinsulinism.

Artwork by Paul Davies

Diabetes to Follow?

The next step in this tragic process is indeed diabetes, a disease that's epidemic among the overweight.[1]

In this situation, the first sign of diabetes is often that the obese person, who's never been able to lose weight, starts losing weight inexplicably. That's because blood sugar is no longer being converted into energy or body fat. Insulin, that crucial fat-producing hormone, has been reduced to impotence.

Diabetes is a heavy-duty illness, not only vastly increasing the risk of heart disease, but having long-term adverse effects on the eyes, kidneys, nervous system, and skin.

A Few More Insulin Problems

Not all fat people reach diabetes, but afflicted as they are with hyperinsulinism, they are in a pre-diabetic condition that has its own significant perils. Those of you who responded "yes" to the B group of symptoms should recognise yourselves.

First, and most noticeable, the persistent bouts of daily fatigue that overweight people can't seem to do anything about; then shakiness and hunger often travelling in company with depression, irritability, and poor mental function. Not only are fat people tired because their cells are not effectively taking in energy, but off and on throughout the day, they are the victims of hypoglycaemia, or low blood sugar, the ironical consequence of consuming too much sugar.

As a man or woman goes deeper into carbohydrate–induced metabolic disorder, hypoglycaemia becomes more and more ingrained. Just a touch of glucose will send insulin pouring forth, dropping blood sugar levels to an abnormal low. If you are a group B person, you become tired, irritable, and hungry. A mid-afternoon attack of hypoglycaemic exhaustion is very typical. This, of course, makes you hungry, you eat more, and the whole sad process goes on. Thus you see that what you thought was compulsivity, a behavioural problem, is really a glucose-triggered mechanism, a metabolic problem. So don't feel so guilty.

There is more to say about hypoglycaemia and I'll be doing that in Chapter 11, when I describe it as one of the branches of a very prevalent modern epidemic, which I call Diet-Related Disorder.

Meanwhile, let me point out that your high insulin levels have other sad results.

* Insulin increases salt and water retention recipe for both hypertension and continued overweight.
* Insulin aggravates hypertension by increasing the responsiveness of arteries to the effects of adrenaline.
* Insulin affects the body's supply of neurotransmitters and can cause sleep disorders.
* Insulin provokes the liver into producing more LDL cholesterol. It may be one of the most significant components in the cholesterol/heart disease connection. Since obesity and high insulin travel in company, this is probably the reason why overweight is such a major risk factor for a heart attack.

Enormous Effects

So you see that when we talk about blood sugar disorders we have a condition that can radically affect an individual's physical and mental states. Women with severe premenstrual syndrome often find, for instance, that a change of diet will correct the underlying hypoglycaemia that can fiercely exacerbate this hormonal condition. When their next menstrual period comes around, they often find they've dramatically improved.

But let's look at hypoglycaemia and its frequent follow up disease, diabetes, in some sort of logical order and try to understand their mechanics.

First There's "Low Blood" Sugar

As I mentioned earlier, your blood glucose powers most of what your body does, as well as fuels your brain. Anytime you're feeling good, you can take it as given that your body is working off of optimal quantities of glucose (or ketone bodies, if you're in ketosis).

Hypoglycaemia (low blood sugar) is not a good thing, but what is hypoglycaemia? The word itself is Greek, derived from hypo meaning 'under,' glykis meaning 'sweet,' and aemia meaning 'in the blood.' Too little sugar in the blood. That sounds clear, but what it demonstrates is that the word hypoglycaemia is actually a misnomer.

Stick with this literal translation, and you will assume it's the opposite of diabetes, which you probably remember involves too much sugar in the blood. You may have heard it said of a diabetic that he's "spilling sugar in his urine." That is indeed the product of excess – and yet the fact is that, far from being opposites, hypoglycaemia and diabetes are actually successive stages of the same disease.

The proper term for describing the hypoglycaemic's real problem is "unstable blood sugar," for it is the overreaction of the glucose mechanism (going up too high and then dropping too far and too fast) that explains the hypoglycaemic's problems.

One of the most intriguing evidences for the hypoglycaemia-diabetes connection was found by scientists in the 1960s.[2] These researchers studied the offspring of two diabetic parents – people who were almost by definition, pre-diabetic. They found a classic series of abnormalities in these patients. First came hypoglycaemia – a sharp drop on the glucose tolerance curve I showed you in Chapter 4. Years would pass. Then these subjects, still hypoglycaemic, showed elevations of their blood sugar readings within an hour after glucose was administered. These elevations lasted 2 hours, then 3 hours. Finally, the very high blood sugar readings of early diabetes occurred throughout the test and throughout the day.

What happened was this: In the early stages, these individuals, genetically sensitive to any abnormalities of blood glucose, were reacting to the high levels of serum glucose that their diet produced by manufacturing large quantities of insulin and forcing the glucose down. This led to the typical hypoglycaemic curve in which blood sugar rises fairly quickly after eating and then falls in the third, fourth, or fifth hour to an unpleasantly low level. It's this fall, too rapid and to somewhat too low a level that constitutes hypoglycaemia, rather than a low level of blood sugar, per se. I make this point because critics of hypoglycaemia have attempted to obfuscate the issue by suggesting that something called low blood sugar is really very rare. As a permanent state of affairs of course, it is. It's a response to glucose rather than a constant deficiency such as you have when your potassium or iron levels are too low.

This early stage is typical of people with insulin resistance – the very people who tend to become fat. People of normal insulin sensitivity tend to stay thin, because just a touch of the "fat producing hormone" is enough to lower their blood glucose to a normal level and more insulin need not be released.

If you're insulin resistant – and you probably are, if you're reading this book to lose weight – then your body at some fairly early stage in your life lost the capacity to respond quickly to insulin. It 'resisted' the insulin, and so the pancreas had to secrete more. The metabolic dynamics of glucose and insulin are thrown awry by this abnormal effort, and the body generally loses its capacity for fine tuning in this essential area. Consequently too much insulin is secreted, and the blood-glucose level is temporarily knocked down to an undesirably low level. The unpleasant symptoms I mentioned at the outset of this chapter are either caused by the fact that the glucose level is too low to supply the brain's needs, or by the adrenalin-like activity initiated to counter-regulate the precipitously falling sugar level.

This is a first step in an unhealthy metabolic path. Eventually, the body can absolutely lose its capacity to produce insulin in the quantities required or its capacity to employ the insulin that's being produced, so that high blood sugar levels result, and the early stages of diabetes are reached.

Lifelong students of diabetes have suggested that the potential for the disease exists in 20% of the population.[3] Keep in mind that most of that 20% is found among the overweight, since, when the final tally is made, 80% of all diabetics are obese. Some studies have suggested that, if you're significantly overweight, your chances of becoming diabetic will be one in two.

And After Hypoglycaemia, Diabetes?

Amazingly enough, many specialists have managed to suggest precisely the wrong diet for their hypoglycaemics, pre-diabetics, and diabetics. I have treated hundreds of patients with Type II diabetes who were put on low-fat, high-carbohydrate diets and consequently had to be on insulin sometimes as much as a hundred units a day to cope with the unnecessary and avoidably high glucose levels that resulted.

I hate to be so cynical as to suggest that proper diet might adversely affect the thoroughly profitable administration of insulin and oral diabetic drugs, but I will certainly say that if sugar were denounced from the scientific pulpits as if it were sin, it would seriously compromise a mutually supportive food and pharmaceutical industrial culture.

It is difficult to avoid the damning implications of a high-carbohydrate diet, especially with regard to hypoglycaemia and diabetes. As far back as 1970, Muller, Faloona, and Unger wrote in The New England Journal of Medicine of the effectiveness of a low-carbohydrate diet in preventing excess insulin production.[4] Four years later, two German doctors, E. F. Pfeiffer and H. Laube, at an International Symposium on Lipid Metabolism, Obesity, and Diabetes Mellitus presented the results of research indicating that diabetes might not occur at all, if it were not for the effects of sugars and starches on insulin levels. (And for T. L. Cleave's brilliant work on the relation between refined carbohydrates and diabetes see Chapter 16 in this book.)

In 1972, in an intriguing study, A. M. Cohen described in the prestigious American journal, Metabolism, how he and his associates had been able to create an entire strain of diabetic rats in just a few generations by feeding them sugar and selectively breeding the most sugar-susceptible rats.[5] Is this not what is effectively happening to a significant percentage of our 20th-century human population? I do not know if any studies indicate overweight people tend to marry other overweight people but if that were the case then they would be selectively breeding for a susceptibility to diabetes provoked by our culture of refined carbohydrates.

Other studies, especially a number carried out on rats from 1964 to 1982, have demonstrated, almost beyond the possibility of contradiction, how the whole process begins with a deterioration of glucose tolerance generally compensated for by hyperinsulinism and continues grimly on toward diabetes.[6]

References

1. Bernstein, Richard K., Diabetes Type II, New York, Prentice Hall Press, pp. 32-33, 1990. Also: Ferrannini, E., et al., Essential Hypertension: an insulin resistance state, Journal of Cardiovascular Pharmacology, 15 (supplement 5), pp. S18-S25, 1990.
2. Ricketts, H. T. et al., Biochemical studies of pre-diabetes, Diabetes 15(12), pp. 880-8, 1966.
3. Ezrin, Calvin, and Kowalski, Robert. The Endocrine Control Diet, New York, Harper and Row, 1990.
4. Muller, W. A. et al., The influence of the antecedent diet upon glucagon and insulin secretion, New England Journal of Medicine 285, pp.1450-4, 1971.
5. Cohen, A.M., Senate Hearings, April 30, 1973.
6. Jarrett, R. J. et al., Glucose tolerance and blood pressure in two population samples: their relation to diabetes mellitus and hypertension, International Journal of Epidemiology 7, pp. 15-24, 1978. Also: Wright, D.W. et al., Sucrose-induced insulin resistance in the rat: modulation by exercise and diet, The American Journal of Clinical Nutrition 38 pp. 879-883, 1983.

Also: Reaven, G.M. et al. Characterization of a model of dietary-induced hypertriglyceridemia in young, non-obese rats, Journal of Lipid Research 20 pp. 371-378, 1970.
Also: Zavaroni, I, et al Effect of fructose feeding on insulin secretion and insulin action in the rat, Metabolism 29 pp. 970-973, 1980.
Also: Hwang, I.S. et al. Fructose-induced insulin and hypertension in rats, Hypertension 10 pp. 512-516, 1987.
Also: Reaven, G.M. Insulin independent diabetes mellitus: metabolic characteristics, Metabolism 29 pp. 445-454, 1980.